Vinnitsa National Medical University
Course of Neurosurgery
Methodological recommendations on the theme:
Tumours of a spinal cord. Classification. Peculiarities of clinical course depending on
localization of a tumour, and character of its growth.
Traumas of the spine and spinal cord. Pathogenesis. Classification. Principles of
rendering the urgent aid at a pre-hospital stage. Indications to a surgery.
Approved at a methodological meeting of the
department of Neurosurgery
"28" _08_ 2008.
The minute № 1
Head of the department
Professor
Tsymbaluk V.I.
Kyiv – 2008
THEME of the class: “Tumours of a spinal cord. Classification. Peculiarities of
clinical course depending on localization of a tumour, and character of its growth.
Traumas of the spine and spinal cord. Pathogenesis. Classification. Principles of
rendering the urgent aid at a pre-hospital stage. Indications to a surgery.
Duration of the class: 2,7 hours.
(For students)
1. Importance of the theme: Pathology of the spine and spinal cord of tumoral and
traumatic character is significant general medical and social problem. The doctor
should be able to put the preliminary clinical diagnosis in primary inspection of the sick
spine with pathology and the spinal cord and to render adequate medical aid.
2. The aims of the class:
2.1.
The practical aims:
To acquaint students with classification of tumours of the spinal cord, classification
of traumas of the spine and spinal cord.
I level
- the student should know the basic clinical signs of tumours of the spine with
compression of the spinal cord, the basic clinical signs of traumatic damage of
the spine and spinal cord.
II level
- the student should be able to examine the patient with a pain syndrome in the
area of the spine, to diagnose a pathology of the intervertebral disk, to plan
examination and adequate treatment.
III level
- to teach the student to examine the sick spine with a pathology and the spinal
cord.
2.2.
IV level
The educational aims: To take part in formations principles of deontology medical
ethics, professional responsibility in general and in contact with patients with a
vertebral - spinal pathology.
3. Interdisciplinary integration.
Disciplines
To know
To be able
2
1 PREVIOUS:
Human anatomy
Anatomy of the spine and
spinal cord.
The topographer. Anatomy To know the basic surgical
with operative surgery.
approaches in pathology of
the spine with the purpose
of decompression of the
spinal cord.
Nervous diseases
To know clinical signs of
transversal affection of the
spinal cord at various levels.
Orthopedics
and
traumatology
To know peculiarities of
clinical
course
and
additional
methods
of
investigation in trauma of
INTRADISCIPLINARY
the spine at various levels.
INTEGRATION:
Congenital pathology of the
Nervous diseases
spine and spinal cord,
clinical signs of tumours of
the spinal cord, pathology
of intervertebral disks with
signs of a radicular pain
syndrome.
4.
To state principles of the
basic surgical approaches in
pathology of the spine and a
spinal cord.
To be able to examine the
patient, to study the
psychoneurologic status of
patients with pathology of
the spine and spinal cord.
To be able to take an
anamnesis, to carry out
general clinical inspection
and
to
plan
special
inspection of the patients
with pathology of the spine
and spinal cord.
The contents of the class. At the practical class classification, clinical course of
tumours of the spinal cord are considered depending on histological structure, localization
and the level of affection of the spinal cord. Indications and contra-indications to carrying
out special additional methods of examination are discussed. Principles of surgery of
tumours of the spinal cord. Radical and palliative operations. Complications and their
preventive measures.
Traumatic affection of the spine and spinal cord. Classification. The closed and open
damages of the spine. Rendering the urgent aid at stages of evacuation. Transportation of
patients. Kinds of traumatic damages of the spinal cord. Modern methods of diagnostics.
Indications to surgery and its principles. Early and late complications, their preventive
measures and treatment. A rehabilitation and social readaptation of patients with damages
of the spine and spinal cord.
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TRAUMA OF THE SPINE AND SPINAL CORD
Mechanisms of Spine and Spinal Cord Injury. Although trauma may involve the
spinal cord alone, the vertebral column is almost invariably injured at the same time. A
useful classification of spinal injuries is one that divides them into fracture-dislocations,
pure fractures, and pure dislocations. The relative frequency of these types is about 3:1:1.
Except for bullet, shrapnel, and stab wounds, a direct blow to the spine is a relatively
uncommon cause of serious spinal cord injury. One such effect is embolism of disc
material, in which nucleus pulposus is propelled under pressure into the adjacent
vasculature of the cord. In civilian life, most spinal injuries are the result of force applied
at a distance. All three types of spinal injury mentioned above are produced by a similar
mechanism, usually a vertical compression of the spinal column to which anteroflexion is
almost immediately added (anterohyperflexion injury); or, the mechanism may be one of
vertical compression and retrohyperflexion (commonly referred to as hyperextension). The
most important variables in the mechanics of vertebral injury are the nature of the bones at
the level of the injury and the intensity, direction, and point of impact of the force.
When the cervical spine is sharply retroflexed, the spinous and articular processes of
the midcervical vertebrae (C4 to C6) are forced together, and these, now acting as a
fulcrum, cause a separation between the vertebral body and the adjacent lower
intervertebral disc. This results in dislocation, and the cord is caught between the laminae
of the lower vertebra and the body of the higher one. Depending upon the intensity of the
driving force, the separation may increase, with rupture of the anterior ligament.
Hyperextension injury to the spinal cord may occur without apparent damage to the
vertebrae, being caused by a sudden inward bulge of the ligamentum flavum. Damage to
the central cord is usually due to an extension injury.
In the case of severe forward flexion injury, the head is bent sharply forward when
the force is applied. The adjacent vertebrae are forced together at the level of maximum
stress. The anterior-inferior edge of the upper vertebral body is driven into the one below,
sometimes splitting it in two. The posterior part of the fractured body is displaced
backward and compresses the cord. Concomitantly, there is tearing of the interspinous and
posterior longitudinal ligaments. Less severe degrees of anteroflexion injury produce only
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dislocation. Vulnerability to the effects of anteroflexion and retroflexion injuries is
increased by the presence of cervical spondylosis or ankylosing spondylitis or a congenital
stenosis of the spinal canal.
The spinal cord may be damaged without radiologic evidence of fracture or
dislocation, particularly in children, but sometimes one cannot determine the full extent of
spinal injury even at autopsy, because of the difficulty in examining the vertebrae.
Computed tomography, MRI, and lateral spine films are all satisfactory means of
demonstrating the vertebral injury, but the tearing of ligaments from vertebral dislocation
can only be inferred from the spinal displacement. Radiologic studies during cautious
flexion or extension of the neck are the only way one can demonstrate instability from
ligamentous injury alone.
Another mechanism of cord and root injury, involving extremes of extension and
flexion of the neck, is so-called whiplash or recoil injury. This type of injury is most often
the result of an automobile accident. When a vehicle is struck sharply from behind, the
head of the occupant is flung back uncontrollably; or, if a fast-moving vehicle stops
abruptly, there is sudden forward flexion of the neck, followed by retroflexion.
Occipitonuchal and sternocleidomastoid muscles and other supporting structures of the
neck and head are affected much more often than the spinal cord or roots. Nevertheless, in
rare instances, quadriparesis, temporary or permanent, results from a violent whiplash
injury. The exact mechanism of neural injury in these circumstances is not clear; perhaps
there is a transient posterior dislocation or momentary retropulsion of the intervertebral
disc into the spinal canal. Again, the presence of a congenitally narrow cervical spinal
canal or of spinal diseases such as cervical spondylosis, rheumatoid arthritis, or ankylosing
spondylitis adds to the hazard of damage to the cord or roots. Spondylitic symptoms may
be aggravated. Also, there are examples of spinal cord compression that result from the
persistent hyperextension of the cervical spine during a protracted period of coma. Arterial
hypotension may be an added factor in particular instances. This combination accounts for
some of the cases of quadriplegia in opiate or other drug addicts following a period of
sustained unresponsiveness.
5
A special type of spinal cord injury, occurring most often in wartime, is one in
which a high-velocity missile penetrates the vertebral canal and damages the spinal cord
directly. In some cases the missile strikes the vertebral column without entering the spinal
canal but virtually shatters the contents of the dural tube or produces lesser degrees of
impairment of spinal cord function. Rarely, the transmitted shock wave will cause a
paralysis of spinal cord function that is completely reversible in a day or two (spinal cord
concussion). This latter condition may also be produced by forceful falls flat on the back,
as occurs not infrequently in athletes engaged in contact sports or in falls from a ladder.
Little is known of the underlying pathologic changes. Acute traumatic paralysis may also
be the consequence of a vascular mechanism. As mentioned earlier, fibrocartilaginous
emboli from an intervertebral disc that has ruptured into radicular arteries and/or veins of
the spinal cord may cause infarction. Or, a traumatic dissecting aneurysm of the aorta may
occlude the segmental arteries of the spinal cord.
The usual circumstances of spinal cord injury have been motor vehicle accidents,
falls (mainly during a state of alcoholic intoxication), gunshot or stab wounds, diving
accidents, motorcycle accidents, crushing industrial injuries, and birth injury, in that order
of frequency. The majority of the fatal cases were associated with fracture dislocations or
dislocations of the cervical spine. Respiration is paralyzed by lesions of C1, C2, and C3
segments. Among nonfatal cases, fracture-dislocation of the lower cervical spine is the
most frequent established mechanism of spinal cord injury in civilian life. In the United
States, the annual incidence of spinal cord injury is from 5 to 5.5 cases per 100,000
population. Males predominate (4:1). Each year about 3500 persons die in close relation to
their injury, and another 5000 are left with complete or nearly complete loss of spinal cord
function.
Pathology of Spinal Cord Injury. As a result of squeezing or shearing of the spinal
cord, there is destruction of gray and white matter and a variable amount of hemorrhage,
chiefly in the more vascular central parts. These changes are maximal at the level of injury
and one or two segments above and below it. Rarely is the cord cut in two, and seldom is
the pia-arachnoid lacerated. The condition is best designated as traumatic necrosis of the
spinal cord tissue. Separation of pathologic entities such as hematomyelia, concussion,
6
contusion, and hematorrhachis (bleeding into the spinal canal) that are concomitant is of
little value either clinically or pathologically. As a lesion heals, it results in a gliotic focus
or cavitation with variable amounts of hemosiderin and iron pigment. Progressive
meningeal fibrosis and a tension syringomyelia will sometimes develop and lead to a
delayed central cord syndrome.
In most traumatic lesions, the central part of the spinal cord with its vascular gray
matter suffers greater injury than the peripheral parts. And in some instances, the lesion is
virtually restricted to the anterior and posterior gray matter, giving rise to segmental
weakness and sensory loss in the arms with few long tract signs. This has been called the
central cervical cord syndrome (or Schneider syndrome, see further on). Fragments of the
syndrome are not uncommon as transient phenomena that reverse over several days.
As with most lesions, the total clinical effect is compounded of an irreversible
structural component and a reversible disorder of function, each of which may vary in
degree. The extent and permanence of the clinical manifestations are determined by the
relative proportions of these two elements.
Clinical Effects of Spinal Cord Injury. When the spinal cord is suddenly and
completely or almost completely severed, three disorders of function are at once evident:
(1) all voluntary movement in parts of the body below the lesion is immediately and
permanently lost; (2) all sensation from the lower (aboral) parts is abolished; and (3) reflex
functions in all segments of the isolated spinal cord are suspended. The last effect, called
spinal shock, involves tendon as well as autonomic reflexes; it lasts for weeks to months
and is so dramatic that Riddoch used it as a basis for dividing the clinical effects of spinal
cord transection into two stages: (1) spinal shock or areflexia and (2) heightened reflex
activity. The separation of these two stages is not as sharp as this statement might imply
but is nevertheless fundamental. Less complete lesions of the spinal cord may result in
little or no spinal shock, and the same is true of any type of lesion that develops slowly.
Stage of Spinal Shock or Areflexia. The loss of motor function at the time of injury
quadriplegia (better termed tetraplegia) with lesions of the fourth to fifth cervical
of bladder and bowel, gastric atony, loss of sensation below the level corresponding to the
7
spinal cord lesion, muscular flaccidity, and complete or almost complete suppression of all
spinal segmental reflex activity below the lesion. The neural elements below the lesion fail
to perform their normal function because of their sudden separation from those of higher
levels. Impaired also in the segments below the lesion is the control of autonomic function.
Vasomotor tone, sweating, and piloerection in the lower parts of the body are temporarily
lost. Systemic hypotension may be severe and contribute to the spinal cord damage. The
lower extremities lose heat if left uncovered, and they swell if dependent. The skin is dry
and pale, and ulcerations may develop over bony prominences. The sphincters of the
bladder and the rectum remain contracted to some degree due to the loss of inhibitory
influence of higher central nervous system centers but the detrusor and smooth muscle of
the rectum are atonic. Urine accumulates until the intravesicular pressure is sufficient to
overcome the sphincters; then driblets escape (overflow incontinence). There is also
passive distention of the bowel, retention of feces, and absence of peristalsis (paralytic
ileus). Genital reflexes (penile erection, bulbocavernosus reflex, contraction of dartos
muscle) are abolished or profoundly depressed.
The duration of the stage of complete areflexia varies greatly. In a small number it is
permanent, or only fragmentary reflex activity is regained many months or years after the
injury. In such patients the spinal segments below the level of transection may have
themselves been injured perhaps by a vascular mechanism, although this explanation is
unproven. More likely there is a loss of the brainstem-spinal facilitatory mechanisms and
an increase in inhibitory activity in the isolated segments as indicated below. In some
patients, minimal genital and flexor reflex activity can be detected within a few days of the
injury. In the majority of patients, this minimal reflex activity appears within a period of 1
to 6 weeks. Usually the bulbocavernosus reflex is the first to return.
The explanation of spinal shock, which is brief in submammalian forms and more
lasting in higher mammals, especially in primates, is believed to be the sudden interruption
of suprasegmental descending fiber systems that normally keep the spinal motor neurons
in a continuous state of subliminal depolarization (ready to respond). In the cat and
monkey, Fulton found the facilitatory tracts in question to be the reticulospinal and
vestibulospinal. Subsequent studies showed that in monkeys, some degree of spinal shock
8
can result from interruption of the corticospinal tracts alone. This cannot be the significant
factor, however, at least in humans, because spinal shock may be very mild or inevident as
a result of acute cerebral and brainstem lesions that interrupt the corticospinal tracts. F
waves of the isolated cord are suppressed. Interest in recent years has focused on a
possible role for neurotransmitters (catecholamines, endorphins, substance P, and 5hydroxytryptamine). The claim that naloxone and the endogenous opiate antagonist
thyrotropin releasing factor might reduce the extent of an acute spinal cord lesion has not
been corroborated. Clonidine, a noradrenergic receptor activator is reported to reduce
flexor spasms and spasticity and to restore the balance between excitatory and inhibitory
activity, allowing the spinal reflex generator for locomotion to function.
Stage of Heightened Reflex Activity. Usually, after a few weeks, the reflex
responses to stimulation, which are initially minimal and unsustained, become stronger
and more easily elicitable and come to include additional and more proximal muscles.
Gradually the typical pattern of heightened flexion reflexes emerges: dorsiflexion of the
big toe (Babinski sign); fanning of the other toes; and later, flexion or slow withdrawal
movements of the foot, leg, and thigh with contraction of the tensor fascialata (triple
flexion). Tactile stimulation of the foot may suffice as a stimulus, but a painful stimulus is
more effective. The Achilles reflexes and then the patellar reflexes return. Retention of
urine becomes less complete, and at irregular intervals urine is expelled by active
contractions of the detrusor muscle. Reflex defecation also begins. After several months
the withdrawal reflexes become greatly exaggerated, to the point of flexor spasms, and
may be accompanied by profuse sweating, piloerection, and automatic emptying of the
bladder (occasionally of the rectum). This is the "mass reflex," which is evoked by
stimulation of the skin of the legs or by some interoceptive stimulus, such as a full bladder.
Varying degrees of heightened flexor reflex activity may last for years. Heat-induced
sweating is defective, but reflex-evoked ("spinal") sweating may be profuse. Presumably,
in such cases the lateral horn cells in much of the thoracic cord are still viable and
disinhibited. Above the level of the lesion, thermoregulatory sweating may be exaggerated
and is accompanied by cutaneous flushing, pounding headache, hypertension, and reflex
bradycardia. This latter syndrome ("autonomic dysreflexia") is episodic and occurs in
9
response to a particular stimulus, such as a distended bladder or rectum. It has been
ascribed to the reflex release of adrenalin from the adrenal medulla and of noradrenalin
from the disinhibited sympathetic terminals caudal to the lesion.
Extensor reflexes eventually develop in most cases, but they do not lead to the
abolition of the flexor reflexes. The overactivity of extensor muscles may appear as early
as 6 months after the injury, but this only happens, as a rule, after the flexor responses are
fully developed. Extensor responses are at first manifest in certain muscles of the hip and
thigh and later of the leg. In a few patients extensor reflexes are organized into support
reactions sufficient to permit spinal standing.
From these observations one would suspect that the ultimate posture of the legs
flexion or extension does not depend solely on the completeness or incompleteness of the
spinal cord lesion. The development of paraplegia in flexion relates also to the level of the
lesion, being seen most often with cervical lesions and progressively less often with more
caudal ones. Repeated flexor spasms, which are more frequent with higher lesions, and the
ensuing contractures ultimately determine a fixed flexor posture. Conversely, reduction of
flexor spasms by elimination of nociceptive stimuli (infected bladder, decubiti, etc.) favors
an extensor posture of the legs (paraplegia in extension). The positioning of the limbs
during the early stages of paraplegia greatly influences their ultimate posture. Thus,
prolonged fixation of the paralyzed limbs in adduction and semiflexion favors subsequent
paraplegia in flexion. Placing the patient prone or placing the limbs in abduction and
extension facilitates the development of predominantly extensor postures. Nevertheless,
strong and persistent extensor postures are observed only with partial lesions of the spinal
cord.
Of some interest is the fact that many patients report sensory symptoms in segments
of the body below the level of their transection. Thus, a tactile stimulus above the level of
the lesion may be felt below the transection (synesthesia). Patients describe a variety of
paresthesias, the most common being a dull, burning pain in the lower back and abdomen,
buttocks, and perineum. We have encountered patients in whom aching testicular or rectal
pain were the main problem. The pain may be intense and last for a year or longer, after
which it gradually subsides. It may persist after rhizotomy but can be abolished by
10
anesthetizing the stump of the proximal (upper) segment of the spinal cord, according to
Pollock and his collaborators. Transmission of sensation over splanchnic afferents to
levels of the spinal cord above the lesion, the conventional explanation, is therefore not the
most plausible one.
The overactivity of neurons in the isolated segments of the spinal cord has several
explanations. One assumes that suprasegmental inhibitory influences have been removed
by the transection, so that afferent sensory impulses evoke exaggerated nocifensive and
phasic and tonic myotatic reflexes. But isolated neurons also become hypersensitive to
neurotransmitters.
Various combinations of residual deficits (lower and upper motor neuron and
sensory) are to be expected. Some of the resulting clinical pictures are complete or
incomplete voluntary motor paralysis; a flaccid atrophic paralysis of upper limb muscles
(if appropriate segments of gray matter are destroyed) with spastic weakness of the legs
(amyotrophy with spastic paraplegia in flexion or extension); a partial or complete BrownSequard syndrome; and each of these with variable sensory impairment in the legs and
arms. High cervical lesions may result in extreme and prolonged tonic spasms of the legs
due to release of tonic myotatic reflexes. Under these circumstances, attempted voluntary
movement may excite intense contraction of all flexor and extensor muscles lasting for
several minutes. Segmental damage in the low cervical or lumbar gray matter, destroying
inhibitory Renshaw neurons, may release activity of remaining anterior horn cells, leading
to spinal segmental spasticity. Any residual symptoms persisting after 6 months are likely
to be permanent, although in a small proportion of patients some return of function
(particularly sensation) is possible after this time. Loss of motor and sensory function
above the lesion, coming on years after the trauma, occurs occasionally and is due to an
enlarging cavity in the proximal segment of the cord.
Central Cord Syndrome of Schneider and "Cruciate Paralysis". In the acute
central cord lesion, the loss of motor function is characteristically more severe in the upper
limbs than in the lower ones and particularly severe in the hands. Bladder dysfunction with
urinary retention occurs in some of the cases and sensory loss is often slight (hyperpathia
over the shoulders and arms may be the only sensory abnormality). The destruction of
11
gray matter (motor and sensory neurons) may leave an atrophic, areflexive paralysis and a
segmental loss of pain and thermal sensation. Retroflexion injuries of the head and neck
are the ones most often associated with this central cord syndrome, but hematomyelia,
necrotizing myelitis, fibrocartilagenous embolism, and possibly infarction due to
compression of the vertebral artery in the medullary-cervical region are other causes.
4 % of patients who survive high cervical cord injuries demonstrate what these
authors refer to as "cruciate paralysis." The latter state is similar to the central cord
syndrome except that the weakness is even more selective, being practically limited to the
arms, a feature that is attributable to the segregation of corticospinal fibers to the arms
(rostral) and to the legs (caudal) within the decussation. The patients described in the
literature have had injuries, basically contusions, of the C1-C2 region. The arm weakness
may be asymmetrical or even unilateral; sensory loss is inconsistent.
Examination of the Spine-Injured Patient. The level of the spinal cord and
vertebral lesions can be determined from the clinical findings. A complete paralysis of the
arms and legs usually indicates a fracture or dislocation at the fourth to fifth cervical
vertebrae. If the legs are paralyzed and the arms can still be abducted and flexed, the lesion
is likely to be at the fifth to sixth cervical vertebrae. Paralysis of the legs and only the
hands indicates a lesion at the sixth to seventh cervical level. Below the cervical region,
the spinal cord segments and roots are not opposite their similarly numbered vertebrae.
The spinal cord ends opposite the first lumbar interspace. Vertebral lesions below this
point give rise predominantly to cauda equina syndromes; these carry a better prognosis
than injuries to the lower thoracic vertebrae, which involve both cord and multiple roots.
The level of sensory loss on the trunk, determined by perception of pinprick, is also an
accurate guide to the level of the lesion, with a few qualifications. With lesions of the
lower cervical cord, even if complete, sensation may be preserved down to the nipple line,
because of the contribution of the C3 and C4 cutaneous branches of the cervical plexus,
which innervate skin below the clavicle. Rarely, a lesion will involve only the outermost
fibers of the spinothalamic pathways, sparing the innermost ones, in which case the
sensory level (to pain and temperature) will be below the level of the lesion. In all cases of
12
spinal cord and cauda equina injury, the prognosis for recovery is more favorable if any
movement or sensation is elicitable during the first 48 to 72 h.
If the spine can be examined safely, it should be inspected for angulations or
irregularities and gently percussed to elicit signs of bony injury. Collateral injury of the
thorax, abdomen, and long bones must always be sought, to direct early radiologic studies
and detect serious complications such as pneumothorax, splenic rupture, or fat embolism.
Management of Spinal Injury. In all cases of suspected spinal injury, the
immediate concern is that there be no movement (especially flexion) of the cervical spine
from the moment of the accident. The patient should be placed supine on a firm, flat
surface (with one person assigned to keeping the head immobile) and should be
transported by a vehicle that can accept the litter. Preferably, the patient should be
transported by an ambulance equipped with spine boards, to which the head is rigidly
fixed by straps. The latter provide a more effective means of immobilization than sandbags
or similar objects placed on each side of the head and neck. On arrival at the hospital, it is
useful to have the patient remain on the backboard until a lateral film and MRI of the
cervical spine have been obtained.
A careful neurologic examination with detailed recording of motor, sensory, and
sphincter function is necessary to follow the clinical progress of spinal cord injury. A
common practice is to define the injury according to the standards of the American Spinal
Injury Association and to assign the injury to a point on the Frankel Scale.
Complete: motor and sensory loss below the lesion
Incomplete: some sensory preservation below the zone of injury
Incomplete: motor and sensory sparing, but the patient is nonfunctional
Incomplete: motor and sensory sparing and the patient is functional (stands and
walks)
Complete functional recovery: reflexes may be abnormal
Obviously, groups B, C, and D have a more favorable prognosis for recovery of
ambulation than does group A.
13
Once the degrees of injury to spine and cord have been assessed, corticosteroids are
given in high dosage. In patients receiving methylprednisolone (bolus of 30 mg/kg
followed by 5.4 mg/kg every hour), beginning within 8 h of the injury and continuing for
23 h, Bracken and colleagues reported a slight but significant improvement in both motor
and sensory function compared to controls. Naloxone was found to be of no value. Also, in
a small series of patients, the administration of GM1 ganglioside (100 mg intravenously
each day from the time of the accident) was found to enhance ultimate recovery to a
modest degree, but this finding needs to be corroborated.
Next, radiologic examinations are undertaken to determine the alignment of
vertebral bodies and pedicles, compression of the spinal cord or cauda equina due to
malalignment or bone debris in the spinal canal, and the presence of tissue damage within
the cord. The MRI is ideally suited to display these processes but if it is not availble, or if
there is uncertainty regarding cord compression, it is useful to perform myelography with
CT scanning to obtain more detailed views of the spinal subarachnoid space. Instability of
the spinal elements can often be inferred from dislocations or from certain fractures of the
pedicles, pars articularis, or transverse processes, but gentle flexion and extension of the
injured areas must sometimes be undertaken and films obtained in each position.
If the spinal cord injury is associated with vertebral dislocation, traction on the neck
is necessary to secure proper alignment and maintain immobilization. This is best
accomplished by use of a halo brace, which, of all the appliances used for this purpose,
provides the most rigid external fixation of the cervical spine. This type of fixation is
usually continued for 4 to 6 weeks, after which a rigid collar may be substituted.
In general, concerning the early surgical management of spinal cord injury, there
have been two schools of thought. One, represented by Guttmann and others, advocates
reduction and alignment of the dislocated vertebrae by traction and immobilization until
skeletal fixation is obtained, and then rehabilitation. The other school, represented by
Munro and later by Collins and Chehrazi, proposes early surgical decompression,
correction of bony displacements, and removal of herniated disc tissue and intra- and
extramedullary hemorrhage; often the spine is fixed at the same time by a bone graft or
wiring. Most American neurosurgeons take the less aggressive stance, delaying operation
14
or operating only on patients with compound wounds or in those with progression or
worsening of the neurologic deficit despite adequate reduction and stabilization. With
complete spinal cord lesions, most surgeons do not favor surgery.
The results of the conservative and aggressive surgical plans of management have
been difficult to compare and have not been evaluated with modern neurologic techniques.
Collins, a participant in the National Institutes of Health (NIH) study of acute management
of spinal cord injury, concluded that the survival rate was increased as a result of early
surgical stabilization of fractures and fixation of the spine (in addition to the usual
measures for the prevention of respiratory, urinary, and cutaneous complications and the
early institution of rehabilitation measures). Other neurosurgeons, however, have not been
able to document a reduction in neurologic disability as a result of early operation, and
increasingly have inclined toward nonoperative management of both complete and partial
spinal cord lesions (Clark; Murphy et al). In any given case, the approach must be guided
by the particular features of the patient's injuries.
The greatest risk to the patient with spinal cord injury is in the first week or 10 days
when gastric dilatation, ileus, shock, and infection are the main threats to life. The
mortality rate falls rapidly after the first 3 months; beyond this time, 86 % of paraplegics
and 80 % of quadriplegics will survive for 10 years or longer. In children, the survival rate
is even higher. The cumulative 7-year survival rate in spinal cord-injured patients (who
had survived at least 24 h after injury) are 87 %. Advanced age at the time of injury and
being rendered completely quadriplegic were the worst prognostic factors.
The aftercare of patients with paraplegia is concerned with management of bladder
and bowel disturbances, care of the skin, prevention of pulmonary embolism, and
maintenance of nutrition. Decubitus ulcers can be prevented by frequent turning to avoid
pressure necrosis, use of special mattresses, and meticulous skin care. Deep lesions require
debridement and full-thickness grafting. At first continual catheterization is necessary;
then, after several weeks, the bladder can be managed by intermittent catheterization once
or twice daily, using a scrupulous aseptic technique. Close watch is kept for bladder
infection, which is treated promptly should it occur. Bacteruria is common and does not
require treatment with antibiotics unless there is associated pyuria. Morning suppositories
15
and periodically spaced enemas are the most effective means of controlling fecal
incontinence. Chronic pain (present in 30 to 50 % of cases) requires the use of
nonsteroidal anti-inflammatory medication, injections of local anesthetics, and
transcutaneous nerve stimulation. A combination of carbamazepine and either clonazepam
or tricyclic antidepressants may be helpful in cases of burning leg and trunk pain.
Recalcitrant pain may require more aggressive thera A combination of carbamazepine and
either clonazepam or tricyclic antidepressants may be helpful in cases of burning leg and
trunk pain. Recalcitrant pain may require more aggressive therapy, such as epidural
injections of analgesics or corticosteroids, but often even these measures are ineffective.
Spasticity and flexor spasms may be troublesome; oral baclofen, diazepam, or tizanidine
may provide some relief. In permanent spastic paraplegia with severe stiffness and
adductor and flexor spasms of the legs, intrathecal baclofen, delivered by a selfadministered pump in doses of 12 to 400 mg/day, has reportedly been helpful. The drug is
believed to act at the synapses of spinal reflexes. One must always be alert to the threat of
pulmonary embolism from deep-vein thrombi, although the incidence is surprisingly low
after the first several months. Physiotherapy, muscle reeducation, and the proper use of
braces are all important in the rehabilitation of the patient. All this is best carried out in
special centers for rehabilitation of spinal cord injuries.
5. Materials of methodological maintenance of the practical class.
5.1.
Materials of the control of a preparatory stage: questions, tests of the initial level.
5.2.
Materials of methodological maintenance of the basic stage of the class.
5.3.
Materials of the control of the final stage: situational tasks, tests of the final level.
5.4.
Materials of methodological maintenance of self-preparation of students: see
methodological recommendations to independent work of the students.
5.5.
SITUATIONAL TASKS FOR CHECKING OF THE LEVEL OF KNOWLEDGE
OF STUDENTS WITH STANDARD ANSWERS
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№1. The patient developed numbness of the right toes and weakness in left foot, 2 months
later he developed numbness of the left foot and weakness in the right foot. Sensor
disorders spread up, weakness in the lower extremities grew, there was retention of stool.
Objectively: the lower spastic paraplegia, knee and achill reflexes are high, polykinetic,
pathological symptoms of Babinsky, Gordon on either sides. Hypesthesia by conduction
type of the level of Th6 segment. The patient can’t urinate.
Make the preliminary diagnosis, specify the plan of examination.
Answer: the preliminary diagnosis a tumour of the spinal cord at the level of the upper
thoracic part of the spine. The plan of examination: spondylogram in two projections, a
lumbar puncture with liquorodynamic tests.
№2. The patient of 38 years old after lifting weight developed the pain in the lumbar area
with irradiation to a posterior-external surface of the left leg. Because of pains the scope of
movements in the lumbar part of the spine was sharply limited. What preliminary
diagnosis can be made in the patient? Specify the plan of inspection of the patient.
Answer: the preliminary diagnosis is discogenic radiculitis with loss of disk L4-L5. The
plan of inspection consists of spondylogram in two projections, epidurography,
myelography.
№3. The patient of 23 years old on the background of high temperature (39 oС) developed
weakness and numbness in the low extremities. In 2 days active movements in the lower
extremities have completely disappeared, there were the numbness of the lower part of the
body, retention of urine. Objectively: the lower spastic paraplegia, hypalgesia with areas
of hypertension from the level Th6 segment by the conduction type, retention of urine,
pathological symptoms of Babinsky, Oppenheim. Temperature 37.8 oС. Make the
preliminary diagnosis, administer examination and treatment.
Answer: the preliminary diagnosis – arachnomyelitis. Auxiliary methods of investigation
are spondylogram in two projections, a lumbar puncture with liquorodynamic tests.
Treatment – a course of anti-inflammatory therapy.
6. The literature
1. Иргер И.Н. Нейрохирургия, М., Медицина, 1982
2. Лебедев В.В., Быковников Л.Д. Руководство по неотложной нейрохирургии. – М.:
Медицина. – 1987. – 336 с.
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3.
Неврология / Под ред. М.Самуэльса. – М.: Практика, 1997. – 640с.
4.
Цимбалюк В., Хонда О., Третяк І., Авад М. Нейрохірургія. Курс лекцій. –
Київ, 1998. – 206 с.
5. Лукачер Г.Я. « Неврологические проявления остеохондроза позвоночника»,М.,
«Медицина», 1985.
6. Фарбер М.А. и соавторы «Поясничный остеохондроз и его неврологические
синдромы – клиника, диагностика и лечение», Ташкент, «Медицина», 1986.
Additional
7. Лившиц А.В. Хирургия спинного мозга. – М.: Медицина 1990.- 352 с.
The literature for students:
1.
Иргер И.Н. Нейрохирургия, М., Медицина, 1982
2.
Лебедев В.В., Быковников Л.Д. Руководство по неотложной нейрохирургии. –
М.: Медицина. – 1987. – 336 с.
3.
Неврология / Под ред. М.Самуэльса. – М.: Практика, 1997. – 640с.
4.
Цимбалюк В., Хонда О., Третяк І.,Авад М. Нейрохірургія. Курс лекцій. – Київ,
1998. – 206 с.
The task for students’ research.
1. To ground peculiarities of clinical course of tumours of the spinal cord depending on
age of the patient.
2. Significance of deontology in treatment of patients with tumours of the spinal cord.
3. Preventive measures of complications in patients with tumours of the spinal cord.
4. Methods of control of urosepsis.
5. Preventive measures of bed sores in patients with affection of the spinal cord.
(Situational tasks in a theme are enclosed)
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